Berman R S, Frew J D, Martin W
Department of Pharmacology, University of Glasgow.
Br J Pharmacol. 1993 Dec;110(4):1282-4. doi: 10.1111/j.1476-5381.1993.tb13956.x.
Using an in vitro model in which albumin transfer across monolayers of bovine aortic endothelial cells (BAEC) was measured, we have shown that lipopolysaccharide (LPS) induces a concentration-dependent increase in endothelial permeability. This increase was biphasic, having an early peak at 2 h and rising again by 24 h. Both peaks were abolished by polymixin B (PMB) but were unaffected by N omega-monomethyl-L-arginine, N omega-nitro-L-arginine methyl ester or dexamethasone. Furthermore, LPS did not stimulate nitric oxide production by BAEC following 24 h exposure. Thus, the LPS-induced increase in permeability may account for the vascular leakage of septic shock, but the L-arginine-nitric oxide system does not appear to be involved.
通过使用一种体外模型来测量白蛋白穿过牛主动脉内皮细胞（BAEC）单层的转运情况，我们发现脂多糖（LPS）可诱导内皮通透性呈浓度依赖性增加。这种增加是双相的，在2小时时有一个早期峰值，并在24小时时再次升高。两个峰值均被多粘菌素B（PMB）消除，但不受Nω-单甲基-L-精氨酸、Nω-硝基-L-精氨酸甲酯或地塞米松的影响。此外，暴露24小时后，LPS并未刺激BAEC产生一氧化氮。因此，LPS诱导的通透性增加可能是脓毒性休克时血管渗漏的原因，但L-精氨酸-一氧化氮系统似乎并未参与其中。
